Genitourinary alterations in children Pediatric differences: Ability to concentrate urine and promote acid-base balance doesnt occur until

ntil age 6. So they are at increased risk of metabolic acidosis Bladder capacity increases with age: 20-50ml at birth to 700 in adult. (they should have 6-8 wet diapers a day) Control of voiding requires nerve innervation which doesnt begin to develop until age 2 and isnt fully developed until age 4-5. Normal urinary output: o Infants: 2ml/kg/hr o Children: 0.5-1 ml/kg/hr o Adolescents: 40-80 ml/hr o Adults: 30-50 ml/hr Bladder Exstrophy Posterior bladder wall extrudes though the lower abdominal wall. Clinical Manifestation: o Bladder mucosa appears as a mass of bright red tissue o They have continual urine leakage (assess for skin breakdown!!) Surgical Repair: (performed in steps) o 24-48 hours after birth Abdominal wall is closed around the bladder Epispadias is repaired Symphysis pubis is closed. o 2-3 years: Reconstruct the bladder next Reimplant the ureters o You usually make a stoma until they can recreate the bladder. o Want the surgery to be completed before potty training begins!! Nursing care: o Pre-op: Cover mucosa in a sterile wrap. Protect surrounding skin from urine with a skin sealant. o Post-op: Immobilize legs and prevent abduction until closure of the sutures occurs. Hypospadias & Epispadias Urethral meatus is placed on ventral surface of the penis- hypo Urethral meatus is placed on the dorsal surface of the penis-Epi Hypo with Chordee: there is a downward curvature of the penis. You must loosen the muscle to straighten out the penis..

With hypo you usually have patent urinary continence. This may impact fertility. Treatment Hypo: o No circumcision- they use the extra skin during surgery. Surgery: Release chordee, lengthen urethra, position meatus, reconstruct the penis. May leave stent to maintain opening. Complete the surgery before potty training. May not do anything to correct if doesnt cause impairment. Treatment Epi: o Surgery Bladder neck reconstruction. Lengthen the urethra Nursing care for both: o Post-op: Wound and stent care (worried about infection) Pain management around the clock Antibiotics until the stent falls out. Double the diapers, one for poop, the other for urine. Obstructive Uropathy

Structural or functional abnormalities that interrupt urine flow. Often causes hydronephrosis. The babies have small lungs. Hydronephrosis Results in: o Decreased renal fxn(eventually HTN); metabolic acidosis; progressive renal damage; potential infection. o Associated with Vesicourethral reflux. Causes (both): o Congenital lesions o Prune-belly syndrome: no abdominal musculature o Myelomeningocele- causes sensory impairment o Neoplasms- can cause obstruction Treatment: o Surgical correction or diversion: Pyeloplasty- take out obstructed parts and reanastamos the good ones. Urinary incontinence in common post-op. Nursing Care: o Watch for urinary retention o No sports=no trauma.

Urinary Tract Infections: Systemic signs of infection Long-term complications: o Renal scarring, HTN, ESRD Pathophysiology: o Fecal bacteria colonizes on perineal area, it adheres to urinary tract epithelial cells, these migrate up the urethra to the bladder, and causes= Cystitis o The bacteria may migrate up the ureters into the renal parenchyma and cause= pyelonephritis. Predispoising factors: o VUR; UTO;Bacterial colonization in the prepuce of the penis (teach parents about cleaning the foreskin) Clinical Manifestations: o Vary. Fever without a pinpoint origin, straight cath them to test for UTI. o Cystitis (Lower UTI): Frequency, dysuria, urgency, Enuresis o Pyelonephritis (Upper UTI) High fever, chills, flank pain, dehydration o Teach parents about wiping front to back, no bubble baths, wear cotton underwear, empty bladder q3-4h. o Increase fluid intake and flush those suckers out!! Treatment: o Cystitis: 5-7 course of antibiotics Encourage fluid intake o Pyelonephritis: 7-10 day of antibiotics following IV antibiotics for 24-48 hours. Antipyretics. Enuresis Repeated involuntary peeing after the age of potty training completion (~5yoa) Many risk factors Clinical Manifestations: o Cant sense bladder fullness, rush to bathroom dont make it, cant sit still, constant odor of urine. Treatment: o Limit fluids after supper, reassure, void just before bed-time. Nasal sprays can be used occasionally (like when going to a sleep-over) it has an antidiuretic effect. o Tofranil is a TCA. Has an anticholinergic effect. They feel the urge sooner.

Nephrotic Syndrome Characterized by: EDEMA & MASSIVE PROTEINURIA Classifications: o Primary: AKA minimal change nephrotic syndrome (MCNS). Results from disorders in the glomerulus of the kidney. (most common type in children). o Secondary: to systemic disease (Diabetes, sle, Sickle cell.) Patho: o Glomerular insult/injury causes glomerular alteration; This leads to proteinuria and hypoalbumenemia; intravascular fluid migrates into interstitial spaces and this causes hypovolemia; which causes increased renin production which causes increased excretion of aldosterone, which enhances reabsorption of sodium and causes an elevation in cholesterol and triglycerides, leading to hyperlipidemia. Or o Glomerular insult increased permeability proteinuria hypoprotenemia & hypoalbumenemia decreased osmotic pressure edema liver compensation (hyperlipidemia). Also o Immunoglobulins are lost in urine which causes leukopenia and increases susceptibility to infection. & o Liver compensation leads to a hypercoagulable state, which leads to increased susceptibility to venous thrombosis. Cause unknown, thought to be immune related because it sometimes follows URI. Prognosis: o MCNS- good, manage fluid volume and HTN issues. Clinical Manifestations: Primary o Edema, massive proteinuria, increased weight, may elevated BP, decreased UOP, respiratory distress, abd. Pain. Treatment: o Remission induction: 90% go into remission Prednisone: decreased inflammation in glomeruli. Cont for 6 weeks before gradual tapering. Alkylating agent if relapse when steroids withdrawn (to avoid acidosis during withdrawal) Albumin: To pull fluid back in to the vascular space Diuretic therapy to get rid of excess fluid. Oral penicillin because being on prednisone increases susceptibility to infection No added salt diet-dont want them retaining more fluid No live virus vaccines because they are on prednisone therapy. Parents taught: o Daily weights; urine protein dipstick testing at home. Relapse common after ser. Inf.

Acute Renal Failure Prerenal ARF: Something wrong before it gets to the kidney. o Patho: Results from DECREASED RENAL PERFUSION of a normal kidneyischemiacellular swelling, injury, and possible death. Many causes Impaired perfusion caused decreased GFR which causes: Oliguria, azotemia (nitrogen waste in urine); and electrolyte imbalances. Intrinsic ARF: Issue in the kidney o Patho: Results from ISCHEMIC DAMAGE to the kidney tissue. Usually caused by some kind of toxin. This is NOT a perfusion Issue! Postrenal ARF: The kidneys are working fine but there is an obstruction after the kidneys that causes back-up which causes a problem. o Patho: Results from OBSTRUCTION of urine outflow from both kidneys. Patho of Recovery: o Renal endothelial and tubular cells begin to return to normal o Renal function gradually returns o GFR returns to normal before tubular transport mechanisms which causes significant diuresis. Dehydration is a possible danger during the recovery phase. While in renal failure you have overload; during recovery you have dehydration! Manifestations: o GROSS HEMATURIA, HA, edema, INCREASED BUN AND CREATININE Treatment: o Fluid needs (replacement and restriction) o Electrolytes: potassium: restric when level reaches 6. Removal achieved by gastric suctioning, kayexalate, sodium bicard, glucose, insulin. o Electrolytes: Sodium: usually decreased from water overload. Correction usually achieved by restriction/replacement. o Nutrition: Max calories, max protein, low sodium and potassium, fluid restrictions. If febrile give some fluids, if afebrile dont give fluids. Goal is to maintain normal serum sodium concentration: o Increased NA []- give some fluids o Decreased NA []- dont give fluids.

Chronic Renal Failure Irreversible loss of kidney function. Managed with meds and diet. Progresses to end stage renal disease End-Stage Renal Disease (ESRD) Permanent, irreversible loss of kidney function that is not manageable by diet and meds o Management requires dialysis or transplant. Chronic Renal Failure Many causes, may be idiopathic Patho: o Destruction of glomeruli causes: Retention of BUN, Creatinine, K+, and Phosphorus; which leads to hypokalemia andhypocalcemia; which leads to bone and body growth arrest Retention of Urine; which causes edema; which leads to HTN Decreased RBC production; and can lead to anemia Manifestations: o Pale, osteodystrophy, rickets, anemia, HTN, decreased alertness and concentration, HA. Treatment: o CRF: Diet! Diuretics, ANTIHTN, sodium bicarb o ESRD: Dialysis or kidney transplant. GFR is the best measure of kidney function!!! Peritoneal Dialysis o Preferred for children because can be done at home or in ambulatory setting. o Complication includes: peritonitis. Fluid goes in clear, there is a problem if it comes out anything other than clear. o There shouldnt be any pain with this. Hemodialysis o More efficient than peritoneal, but requires close monitoring due to hypotension and rapid changes in fluid and electrolytes. o

Polycystic Kidney Disease Genetic (autosomal recessive and dominant forms) Liver abnormalities are ass. With both types. Dilation of collecting ducts from cellular hyperplasia develops into cysts and becomes fibrous. Not an issue until cyst causes obstructions Treatment is supportive May also have low-set ears, flat nose, small jaw. Hemolytic Uremic Syndrome Most common cause of acute failure in children Characterized by: o HEMOLYTIC ANEMIA o ACUTE RENAL FAILURE o THROMBOCYTOPENIA Patho: o Acute renal failure: Bacteria produces a toxin that damages capillary walls which causes an inflammatory response, which occludes the glomerulus, causing decreased GFR, and leading to Acute renal failure o Anemia: RBCs trying to pass through occluded vessels become fragmented and are removed from circulation in the spleen. o Thrombocytopenia Platelets get trapped in small vessels. Treatment is supportive and preventing further complications Acute postinfectious glomerulonephritis Glomerulonephritis: Group of disorders characterized by inflammatory injury in glomerulus. APIGN: immune rxn to group-A beta-hemolytic strep infection of the throat or skin. Manifestations: o HEMATURIA IS THE CARDINAL SIGN!!!!! o Periorbital and dependent edema o HTN o Pulmonary edema Treatment: o No specific therapy o Anti-HTN Prognosis: o Excellent; Diuresis signals resolution! o Then review structural defects!!!!!!!!!!!!!!!!!!!!!!!!!!!